Article Sidebar
Published:
Sep 16, 2014DOI:
10.4314/tjpr.v13i7.8Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Allicin Protects against Lipopolysaccharide-Induced Acute Lung Injury by Up-Regulation of Claudin-4
Abstract
Purpose: To investigate the effect of allicin, an active component of garlic, on lipopolysaccharide (LPS)- induced acute lung injury.
Methods: Wistar rats were subjected to LPS intravenous injection with or without allicin treatment to induce acute lung injury (ALI) model. Also, A549 cells were stimulated with LPS in the presence and absence of allicin. HE staining was used to detect pathological changes in lung tissues. Enzyme-linked immunosorbent assay (ELISA) was performed to measure cytokine content. Cell viability was measured by CCK-8 and EdU incorporation assay. Genes expression was determined by real time polymerase chain reaction (PCR) and Western blot. Flow cytometry was applied to measure cell apoptosis.
Results: In vivo data showed that pulmonary edema, inflammatory cytokines expression and pathological changes were significantly attenuated in LPS-induced ALI after treatment with allicin (p < 0.05) while in vitro results indicate that allicin administration significantly improved the A549 cell viability in a dose-dependent manner as measured by CCK-8 and EdU incorporation assay. Besides, flow cytometry analysis showed that cell apoptosis rate was significantly reduced in a concentrationdependent manner after allicin injection (30.3 vs. 11.8 %, p < 0.05). At the molecular level, allicin treatment dose-dependently up-regulated claudin-4 expression both in vivo and in vitro (p < 0.05).
Conclusion: The findings indicate that allicin can protect against LPS-induced ALI in vivo and in vitro probably by up-regulation of claudin-4 expression.
Keywords: Allicin, Acute lung injury, Lipopolysaccharide, Claudin-4, Up-regulation, Pulmonary edema, Inflammatory cytukines
